Cellular localization of Y-box binding protein 1 in brain tissue of rats, macaques, and humans

Unkrüer, Bernadette; Pekcec, Anton; Fuest, Christina; Wehmeyer, Andrea; Balda, María S.; Horn, Anja K. E.; Baumgärtner, Wolfgang; Potschka, Heidrun

doi:10.1186/1471-2202-10-28

Cited by 23 publications

(13 citation statements)

References 30 publications

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“…The signal of the immunoperoxidase-treated sections was captured with the computer-assisted imaging system StereoInvestigator 6.0 (Microbrightfield Europe, Magdeburg, Germany) as described previously (Unkruer et al, 2009). The hardware consists of a Leica DMLB microscope (Leica, Bensheim, Germany), a Plan-Neofluar lens (Leica, Bensheim, Germany), a single chip charge coupled device (CCD) color camera (CX9000, Microbrightfield Europe, Magdeburg, Germany), and an AMD Athlon 64 Processor.…”

Section: Immunohistological Evaluationmentioning

confidence: 99%

Modulation of neurogenesis by targeted hippocampal irradiation fails to affect kindling progression

Pekcec

Lüpke²,

Baumann

et al. 2011

Hippocampus

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Changes in the rate of dentate granule cell neurogenesis and in the fate of newborn granule cells have been implicated in the development and progression of epilepsies. Strategies to normalize neurogenesis in chronic epilepsy models are thought to increase our understanding of the functional consequences of aberrant neurogenesis in the epileptic brain. Therefore, we modulated neurogenesis in an amygdala kindling paradigm in rats by targeted irradiation of the hippocampus using a medical linear accelerator device. Selective irradiation normalized the hippocampal cell proliferation rate in kindled animals. Both, in kindled and nonkindled rats the number of BrdU/NeuN-labeled newborn neurons was reduced in response to irradiation. Whereas kindling resulted in a pronounced increase in the number of neuroblasts identified based on doublecortin-labeling, irradiation prevented the expansion of the neuroblast population. Moreover, irradiation counteracted the kindling-associated increase in hilar basal dendrites, and kept the fraction of cells with basal dendrites at control levels. Despite the efficacious modulation of neurogenesis, irradiation did not affect the rate of kindling progression. Both, the number of stimulations as well as the cumulative afterdischarge duration to reach respective seizure stages were comparable in animals with and without irradiation. In addition, pre- and postkindling thresholds as well as seizure parameters recorded at threshold stimulation remained unaffected by irradiation. In conclusion, the fact that the efficacious modulation of neurogenesis by irradiation did not exert any effects on kindling acquisition and kindled seizures suggests that newborn neurons do not critically contribute to the hyperexcitable state in the chronic epilepsy model used.

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Section: Immunohistological Evaluationmentioning

confidence: 99%

Modulation of neurogenesis by targeted hippocampal irradiation fails to affect kindling progression

Pekcec

Lüpke²,

Baumann

et al. 2011

Hippocampus

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“…The immunoreaction was visualized using a corresponding biotin-labeled secondary antiserum and the nickel-intensified diaminobenzidine reaction. Cell counting was done using the computerassisted imaging system, StereoInvestigator 6.0 (Microbrightfield Europe, Magdeburg, Germany), as described recently [16]. Newborn neurons were identified by double labeling of BrdU and NeuN and analyzed using a confocal microscope (Zeiss LSM 410 microscope, Zeiss, Oberkochen, Germany) as described earlier [13,14].…”

Section: Methodsmentioning

confidence: 99%

Polysialic acid affects pathophysiological consequences of status epilepticus

Pekcec

Weinhold²,

Gerardy‐Schahn³

et al. 2010

NeuroReport

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Modulation of the neural cell adhesion molecule by the attachment of polysialic acid residues through the polysialyl-transferase, ST8SiaIV, regulates neuronal plasticity and affects cellular alterations in the epileptic brain. Here, we determined the impact of ST8SiaIV deficiency on the pathophysiological consequences of status epilepticus (SE). ST8SiaIV deficiency reduced the latency to SE induction and increased SE-mediated mortality. Analysis of the doublecortin expression showed a reduced number of neuroblasts as a long-term consequence of SE in ST8SiaIV knockouts. Testing in a battery of different behavioral paradigms indicated that loss of ST8SiaIV affects the long-term behavioral consequences. In summary, the data suggest that the polysialic acid-neural cell adhesion molecule system is a putative target for the modulation of pathophysiological events and affects psychiatric comorbidities in epilepsies.

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“…Neurons show a predomi-nant YB-1 expression adult rat, macaque and human brains. YB-1 has been found to be imperative for the maintenance of mouse neuronal stem cells (Unkrüer et al, 2009). Fotovati et al, (2011 found a high expression of YB-1 in subventricular zone of normal E14 mouse tissues.…”

Section: Yb-1 and Brain Cancermentioning

confidence: 99%

“…In rat brain, the YB-1 is found to be highly expressed in the dentate gyrus, cornuammonis pyramidal cell layer and layer III of the piriformcortex. Neuronal YB-1 expression in explicit brain areas ranges to the adult brain and amounts relevant altitudes in the adult rat, macaque and human brain (Unkrüer et al, 2009). However, a decline in the YB-1 brain expression in the postnatal phase has been described (Funakoshi et al, 2003).…”

Section: Yb-1 and Brain Cancermentioning

confidence: 99%

“…To study YB-1 expression in the brain Unkrüer et al, (2009) transcardially perfused the brain tissue from a six year old adult male macaque (Macaca fascicularis) in 0.1 M phosphate buffer and processed. Other than this, 3 µm thin tissue sections of hippocampus from a former neuropathological study were used to evaluate the YB-1 expression in human brain.…”

Section: Yb-1 and Brain Cancermentioning

confidence: 99%

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Nuclear shuttling of Y Box binding protein-1, its clinical relevance in cancer and as a therapeutic target

Gunasekaran

Nishi

Ravikumar

et al. 2016

Bangladesh J Pharmacol

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Y-box binding protein 1 (YB-1) is an imperative biomarker for the clinical outcome of cancer patients. An overexpression of YB-1 in cancerous and adjoining tissues is an indication of aggressiveness and advanced stages. In normal resting cells, YB-1 is localized in cytoplasm while in stress conditions like cancer, nuclear shuttling of YB-1 takes place. In this review, the clinical importance of YB-1 in different cancers and the mechanism behind YB-1 nuclear shuttling have been discussed in detail. Targeted chemotherapies or molecularly targeted drugs of great importance can target and block specific molecules implicated in tumor growth and progression. YB-1 has been considered as a bonafide oncogene and accumulating evidences show the therapeutic importance of YB-1. Therapeutic strategies targeting YB-1 may improve the survival rate in cancer patients. This review extensively discusses the therapeutic importance of YB-1. Article InfoReceived:16 Mini-reviewThis article was downloaded by you on: Apr 30, 2016 In normal resting cells, full length YB-1 is mainly present in the cytoplasm of cells under stress during pathological conditions including inflammation, oxidative stress and cancer conditions. Particular segment of the YB-1 flips to the nucleus (Koike et al., 1997;Higashi et al., 2011).In this review, with the nuclear shuttling, clinical significance of YB-1 in cancer and as a therapeutic target have been evaluated from the existing literature. The present literature analysis shows the prospective role of YB-1 in cancer progression and drug resistance which could be harnessed to make it a promising therapeutic target. Nuclear shuttling of YB-1Since a number of functions have been assigned to YB-1, therefore, the sub-cellular protein shuttling needs to be highly stringent. In general, specific nuclear export signals and nuclear localization signals (NLS) contribute and direct the multifunctional shuttling and tasking (Bader and Vogt, 2005). Literature suggests three nuclear localization signals in YB-1 i.e. NLS1 (aa149-55), NLS2 (aa185-94) and NLS3 (276-92) (van Roeyen et al., 2013). The NLS3 is bipartite in composition and both the parts are essential for functionality. Irrespective of this, the changes of the spatial organization of 2 parts doesn't affect nuclear shuttling. Both NLS2 and NLS3 are essential for functionality and contain tyrosine residues which are required for phosphorylation. The full length YB-1 phosphorylated at tyrosine 281 in NLS3 has been found to be localized in the nucleus while the unphosphorylated YB-1 localized in the cytoplasm. This indicates that the phosphorylation at T-281 renders complete YB-1 to be localized in nucleus under normal conditions (van Roeyen et al., 2013). At the time of stress or cell stimulation, nuclear flipping of shortened YB-1 having N-terminal portion of the proteins takes place through a highly regulated process (Bader and Vogt, 2005;van Roeyen et al., 2013). Jürchott et al. (2003) suggested that the both C-terminal and cold shock domain of YB...

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Cellular localization of Y-box binding protein 1 in brain tissue of rats, macaques, and humans

Cited by 23 publications

References 30 publications

Modulation of neurogenesis by targeted hippocampal irradiation fails to affect kindling progression

Modulation of neurogenesis by targeted hippocampal irradiation fails to affect kindling progression

Polysialic acid affects pathophysiological consequences of status epilepticus

Nuclear shuttling of Y Box binding protein-1, its clinical relevance in cancer and as a therapeutic target

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